LEARNING DEFICITS AFTER HEMORRHAGE IN RATS
LEARNING DEFICITS AFTER HEMORRHAGE IN RATS
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DOI：
10.1016/j.neuroscience.2010.06.039
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发表时间：
2010-09-15
期刊：
影响因子：
3.3
通讯作者：
Macdonald, R. L.
中科院分区：
文献类型：
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作者：
Jeon, H.;Ai, J.;Macdonald, R. L.
大约50%的蛛网膜下腔出血（SAH）幸存者有认知或神经行为功能障碍。其机制尚不清楚。本研究的特点是在大鼠蛛网膜下腔出血模型的行为缺陷，并与这些变化与组织学改变。视交叉前池注入0.3ml血液诱发SAH。在Morris水迷宫中研究认知和记忆的变化。通过荧光玉和末端脱氧核苷酸转移酶dUTP缺口末端标记（TUNEL）染色评价神经细胞死亡。在大脑中动脉和前动脉的横截面上评估血管痉挛。通过纤维蛋白原染色定量微血栓栓塞。SAH组大鼠逃避潜伏期和游泳距离较对照组明显延长（P
About 50% of subarachnoid hemorrhage (SAH) survivors have cognitive or neurobehavioral dysfunction. The mechanisms are not known. This study characterized behavioral deficits in a rat SAH model, and correlated these changes with histological alterations. SAH was induced by injection of 0.3 ml blood into the prechiasmatic cistern. Cognitive and memory changes were investigated in the Morris water maze. Neuronal cell death was evaluated by fluoro-jade and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. Vasospasm was assessed on cross-sections of middle and anterior cerebral arteries. Microthromboemboli were quantified by fibrinogen staining. Escape latency and swimming distance were significantly increased in rats with SAH as compared to controls (P